Molecule Information
General Information of the Molecule (ID: Mol05212)
Type(s) of Resistant Mechanism of This Molecule
Drug Resistance Data Categorized by Drug
Approved Drug(s)
3 drug(s) in total
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Testicular cancer [.] | [2] | |||
| Resistant Disease | Testicular cancer [.] | |||
| Resistant Drug | Cisplatin | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Experiment for Molecule Alteration |
RT-qPCR with "Low Density Array" | |||
| Experiment for Drug Resistance |
MTT assay | |||
| Mechanism Description | Examining almost all known human micro-RNA species confirmed the miR-371-373 cluster as a promising target for explaining cisplatin resistance, potentially by counteracting wild-type P53 induced senescence or linking it with the potency to differentiate. Moreover, we describe for the first time an association of the up-regulation of micro-RNA species such as hsa-miR-512-3p/-515/-517/-518/-525 and down-regulation of hsa-miR-99a/-100/-145 with a cisplatin resistant phenotype in human germ cell tumors. | |||
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | [3] | |||
| Resistant Disease | Pancreatic ductal adenocarcinoma [ICD-11: 2C10.0] | |||
| Resistant Drug | Gemcitabine | |||
| Molecule Alteration | Expression | Down-regulation |
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| Experimental Note | Identified from the Human Clinical Data | |||
| In Vitro Model | SUIT-2 cells | Pancreas | Homo sapiens (Human) | CVCL_3172 |
| Capan-1 cells | Pancreas | Homo sapiens (Human) | CVCL_0237 | |
| Experiment for Molecule Alteration |
qRT-PCR | |||
| Experiment for Drug Resistance |
Propidium Iodide Assay | |||
| Mechanism Description | They play key roles in regulating the translation and degradation of mRNAs through base pairing to partially complementary sites, predominantly in the 3'-untranslated regions of mRNAs.miR-204 has been also reported to be downregulated in intrahepatic cholangiocarcinoma, and the level of miR-204 expression was inversely correlated with that of Bcl-2 expression, possibly leading to chemotherapeutic drug-triggered apoptosis. | |||
| Drug Resistance Data Categorized by Their Corresponding Mechanisms | ||||
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| Disease Class: Breast cancer [ICD-11: 2C60.2] | [1] | |||
| Resistant Disease | Breast cancer [ICD-11: 2C60.2] | |||
| Resistant Drug | Tamoxifen | |||
| Molecule Alteration | Expression | Up-regulation |
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| Experimental Note | Revealed Based on the Cell Line Data | |||
| Cell Pathway Regulation | PI3K-AKT signalling pathway | Regulation | N.A. | |
| Cell cycle pathways | Regulation | N.A. | ||
| In Vitro Model | MCF-7 cells | Breast | Homo sapiens (Human) | CVCL_0031 |
| Experiment for Molecule Alteration |
qRT-PCR | |||
| Experiment for Drug Resistance |
Cell viability assay; Cell cycle assays; Apoptosis assay | |||
| Mechanism Description | Our findings indicate that tamoxifen-resistant cells express miRNA-519a at high levels, which directly represses the expression of PTEN, RB1, and CDKN1A, central nodes of a dense network, allowing the cells to proliferate, even in the presence of tamoxifen. | |||
References
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